ArticleThe Journal of clinical investigation2022
miR-181b targets semaphorin 3A to mediate TGF-β-induced endothelial-mesenchymal transition related to atrial fibrillation.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Histone modification of endothelial-mesenchymal transition in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Pooled it
- SGLT2 inhibitors: mechanisms, physiology and pharmacology, and clinical applications.Molecular biomedicine · 2026Review
- Gut microbiota-activated PLCγ2 monocytes drive atrial fibrillation.Nature communications · 2026Article
- Relationship between serum circulating Syndecan-1 levels and myocardial fibrosis and major adverse cardiovascular events in elderly patients with atrial fibrillation.Heart and vessels · 2026Article
- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Interstitial cells and arrhythmia.American journal of physiology. Cell physiology · 2026Review
- The Interplay Between Periodontitis and Atrial Fibrillation: Inflammation as a Common Pathophysiological Bridge.International journal of molecular sciences · 2026Review
- Intracavernous Injection of Mechanically Extracted Stromal Vascular Fragments Suppresses Endothelial-Mesenchymal Transformation to Mitigate Erectile Dysfunction in Hypertensive Rats.Stem cells international · 2026Article
- Research Progress of Nerve Injury-Induced Protein 1 in Cardiovascular Diseases.Cardiology research and practice · 2026Review
- Proteome-wide Mendelian randomization identifies drug targets for atrial fibrillation/flutter.BMC cardiovascular disorders · 2025Article
- NAT10 Mediates Cardiac Fibrosis Induced by Myocardial Infarction Through ac4C Modification of TGFBR1 mRNA.Cell biology and toxicology · 2025Article
- Molecular mechanisms and intervention approaches of heart failure (Review).International journal of molecular medicine · 2025Review
- TGF-β-Driven Atrial Fibrosis in Atrial Fibrillation: From Mechanistic Insights to Targeted Therapies.Aging and disease · 2025Review
- Article
- Preliminary analysis of the diagnostic value and mechanism of action of TGFbI and S100A4 in hepatocellular carcinoma.Journal of medical biochemistry · 2025Article
- Angiogenesis in Atrial Fibrillation: A Literature Review.Biomedicines · 2025Review
- Article
- Endothelial-Mesenchymal Transition and Possible Role of Cytokines in Streptozotocin-Induced Diabetic Heart.Biomedicines · 2025Article
- Review
- Translation of pathophysiological mechanisms of atrial fibrosis into new diagnostic and therapeutic approaches.Nature reviews. Cardiology · 2025Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrosis is an essential contributor to atrial fibrillation (AF). It remains unclear whether atrial endocardial endothelial cells (AEECs) that undergo endothelial-mesenchymal transition (EndMT) are among the sources of atrial fibroblasts. We studied human atria, TGF-β-treated human AEECs, cardiac-specific TGF-β-transgenic mice, and heart failure rabbits to identify the underlying mechanism of EndMT in atrial fibrosis. Using isolated AEECs, we found that miR-181b was induced in TGF-β-treated AEECs, which decreased semaphorin 3A (Sema3A) and increased EndMT markers, and these effects could be reversed by a miR-181b antagomir. Experiments in which Sema3A was increased by a peptide or decreased by a siRNA in AEECs revealed a mechanistic link between Sema3A and LIM-kinase 1/phosphorylated cofilin (LIMK/p-cofilin) signaling and suggested that Sema3A is upstream of LIMK in regulating actin remodeling through p-cofilin. Administration of the miR-181b antagomir or recombinant Sema3A to TGF-β-transgenic mice evoked increased Sema3A, reduced EndMT markers, and significantly decreased atrial fibrosis and AF vulnerability. Our study provides a mechanistic link between the induction of EndMT by TGF-β via miR-181b/Sema3A/LIMK/p-cofilin signaling to atrial fibrosis. Blocking miR-181b and increasing Sema3A are potential strategies for AF therapeutic intervention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.